Intra-/extra-vascular hemolysis of sRBCs leads, in addition, to the increase in free Hb and arginase-1 at the vascular level, causing NO depletion, and triggering vasoconstriction, endothelial dysfunction, and vascular remodeling [22]; in addition, Hb and heme groups promote ROS production, erythrocyte and vessel membrane damage, promoting cell adhesion to the endothelium [1]. The gene discussed is GSTM1; the disease is endothelial dysfunction.